Possible involvement of serotonin receptors in the facilitatory effect of a hallucinogenic phenethylamine on single facial motoneurons

1986 ◽  
Vol 64 (10) ◽  
pp. 1302-1309 ◽  
Author(s):  
Nicholas J. Penington ◽  
R. J. Reiffenstein

2,5-Dimemoxy-4-methylamphetamine (DOM, "STP") is a potent hallucinogen, proposed to be a serotonin receptor agonist. Its effects have not previously been tested upon central neurons where serotonin is excitatory and serotonin antagonists are effective. Extracellular single unit recordings were obtained from facial motoneurons in anaesthetized rats, and drugs were applied from five-barrelled micropipettes by iontophoresis. Facial motoneurons were commonly silent. During subthreshold application of glutamate, firing could be induced by dopamine and DOM. As reported by others, serotonin and noradrenaline also excited facial motoneurons under these conditions. Methysergide antagonized responses to serotonin and DOM but not those to noradrenaline; methysergide could not usually discriminate between responses to serotonin and dopamine. Ketanserin reversibly antagonized (but could not discriminate between) responses to serotonin, dopamine, and noradrenaline. Chlorpromazine antagonized responses to dopamine at doses that did not alter serotonin-induced excitation, and responses to DOM were not reduced by doses of chlorpromazine, that had no local anaesthetic effect on action potentials elicited by DOM and serotonin. These results suggest that DOM is an agonist on at least one type of central serotonin receptor. This receptor may also be a ketanserin (5-HT2) binding site.

1973 ◽  
Vol 45 (10) ◽  
pp. 1022-1028 ◽  
Author(s):  
F.W. EICHBAUM ◽  
W.J. YASAKA

2000 ◽  
Vol 41 (5) ◽  
pp. 539-542 ◽  
Author(s):  
MARC VERLEYE ◽  
ISABELLE HEULARD ◽  
JEAN-MARIE GILLARDIN

2000 ◽  
Vol 88 (4) ◽  
pp. 1489-1495 ◽  
Author(s):  
David F. Donnelly ◽  
Ricardo Rigual

A preparation was developed that allows for the recording of single-unit chemoreceptor activity from mouse carotid body in vitro. An anesthetized mouse was decapitated, and each carotid body was harvested, along with the sinus nerve, glossopharyngeal nerve, and petrosal ganglia. After exposure to collagenase/trypsin, the cleaned complex was transferred to a recording chamber where it was superfused with oxygenated saline. The ganglia was searched for evoked or spontaneous unit activity by using a glass suction electrode. Single-unit action potentials were 57 ± 10 (SE) ( n = 16) standard deviations above the recording noise, and spontaneous spikes were generated as a random process. Decreasing superfusate[Formula: see text] to near 20 Torr caused an increase in spiking activity from 1.3 ± 0.4 to 14.1 ± 1.9 Hz ( n = 16). The use of mice for chemoreceptor studies may be advantageous because targeted gene deletions are well developed in the mouse model and may be useful in addressing unresolved questions regarding the mechanism of chemotransduction.


2006 ◽  
Vol 96 (6) ◽  
pp. 2963-2971 ◽  
Author(s):  
Philip M. Lang ◽  
Gila Moalem-Taylor ◽  
David J. Tracey ◽  
Hugh Bostock ◽  
Peter Grafe

Activity-dependent fluctuations in axonal excitability and changes in interspike intervals modify the conduction of trains of action potentials in unmyelinated peripheral nerve fibers. During inflammation of a nerve trunk, long stretches of axons are exposed to inflammatory mediators such as 5-hydroxytryptamine [5-HT]. In the present study, we have tested the effects of m-chlorophenylbiguanide (mCPBG), an agonist at the 5-HT(3) serotonin receptor, on activity- and potential-dependent variations in membrane threshold and conduction velocity of unmyelinated C-fiber axons of isolated rat sural nerve segments. The increase in axonal excitability during application of mCPBG was much stronger at higher frequencies of action potentials and/or during axonal membrane hyperpolarization. The effects on the postspike recovery cycle also depended on the rate of stimulation. At an action potential frequency of 1 Hz or in hyperpolarized axons, mCPBG produced a loss of superexcitability. In contrast, at 0.33 Hz, a small increase in the postspike subexcitability was observed. Similar effects on excitability changes were found when latency instead of threshold was recorded, but only at higher action potential frequencies: at 1.8 Hz, mCPBG increased conduction velocity and reduced postspike supernormality. The latter effect would increase the interspike interval if pairs of action potentials were conducted along several cm in an inflamed nerve trunk. These data indicate that activation of axonal 5-HT(3) receptors not only enhances membrane excitability but also modulates action potential trains in unmyelinated, including nociceptive, nerve fibers at high impulse rates.


1984 ◽  
Vol 62 (4) ◽  
pp. 350-355
Author(s):  
James G. Foulks ◽  
Lillian Morishita

The local anaesthetic effect of cationic, anionic, and neutral alkyl amphipathic agents was similarly enhanced in an apparently nonspecific way by circumstances which modulate electrostatic interactions (acidity, modification of charged groups at the sarcolemmal surface by group-specific reagents, or changes in the calcium concentration), presumably as the result of secondary effects on the conformation of membrane proteins. However, the selective enhancement of the local anaesthetic effect of alkyl trimethylammonium compounds by perchlorate implies a more specific interaction which may influence the penetration of hydrophobic groups into the membrane interior.


1976 ◽  
Vol 54 (6) ◽  
pp. 937-944 ◽  
Author(s):  
J. M. Wright ◽  
B. Collier

The site of neuromuscular blockade induced by clindamycin and lincomycin was studied on isolated nerve and nerve–muscle preparations. Clindamycin (3.6 × 10−3 M) but not lincomycin (up to 1.5 × 10−2 M) had a local anaesthetic effect on a frog desheathed nerve preparation. Clindamycin (8 × 10−4 M) and lincomycin (4 × 10−3 M) depressed the response of the rat diaphragm to nerve stimulation and to direct muscle stimulation in parallel. This indicated that the predominant neuromuscular blocking effect of these antibiotics was due to an effect on the muscle. Clindamycin was fivefold more potent than lincomycin in this effect, and the unionized form of both drugs was the active form. Lincomycin (4 × 10−3 M) but not clindamycin (8 × 10−4 M) also had some depressant effect on nerve–muscle transmission as indicated by the interaction of the effects of the antibiotics and d-tubocurarine. The significance of these findings is discussed in relation to the acute clinical toxicity of these antibiotics.


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